Assessment by autonomic blockade of age-related changes of the sinus node function and autonomic regulation in sick sinus syndrome

Age-related changes of the sinus node (SN) function and the autonomic influence on the SN function were evaluated in 65 patients with sick sinus syndrome (range 14 to 84 years). Heart rate (HR), corrected SN recovery time and sinoatrial conduction time were measured before (basic) and after (intrinsic) autonomic blockade (propranolol 0.2 mg/kg plus atropine 0.04 mg/kg intravenously). Percent of autonomic chronotropies of the SN function were calculated by the following formulas: (1)--(intrinsic HR--basic HR/intrinsic HR) X 100; (2) (intrinsic corrected SN recovery time--basic corrected SN recovery time/intrinsic corrected SN recovery time) X 100; (3) (intrinsic sinoatrial conduction time--basic sinoatrial conduction time/intrinsic sinoatrial conduction time) X 100. Basic HR, basic corrected SN recovery time and basic sinoatrial conduction time did not vary with age. Intrinsic HR decreased with age, but this correlation was weak (r = -0.54, p less than 0.001). Intrinsic corrected SN recovery time and intrinsic sinoatrial conduction time tended to increase with age (r = 0.26, p less than 0.05; r = 0.29, p less than 0.05, respectively). Percent chronotropies of HR, corrected SN recovery time and sinoatrial conduction time were negative values in younger patients and positive values in elderly patients; they correlated positively with age (r = 0.59, p less than 0.001; r = 0.60, p less than 0.001; r = 0.43, p less than 0.001, respectively). Thus, the basic SN function did not change with age, while the intrinsic SN function deteriorated with age.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reproducibility of electrophysiological parameters of sinus node following autonomic blockade

We investigated the reproducibility of sinus node cycle length (SCL), corrected sinus node recovery time (CSRT) and sino-atrial conduction time (SACT) during the control state and following autonomic blockade in 25 patients (mean age: 56.9 ± 13.8 years). Autonomic blockade was induced by i.v. administration of propranolol (0.2 mg/kg) and atropine (0.04 mg/kg). The electrophysiological study was repeated after 24 hr and the results were compared. The patients were divided into two groups: Group 1 (15) with normal and Group 2 (10) with abnormal intrinsic sinus node function. Following autonomic blockade in Group 1 the daily variations in SCL, CSRT and SACT were very slight whereas in Group 2 there was far greater variability in these parameters. However, in the latter group there were no patients who changed their status from prolonged to normal intrinsic CSRT on the second study, whereas SACT changed its status in 2 patients. In Group 1 the daily variations in sinus node parameters were much slighter following autonomic blockade than during the control state. In Group 2 the variations were very similar during control and following autonomic blockade.These data suggest that: (1) following autonomic blockade the reproducibility of sinus node parameters is very good in Group 1, whereas in Group 2 several patients show marked daily variations in sinus node parameters; (2) following autonomic blockade the sinus node electrophysiological parameters are meaningful in diagnosing an involvement of intrinsic sinus node function; and (3) in patients with abnormal sinus node parameters during control state, but with normal intrinsic sinus node function, the daily variations are mainly due to change in autonomic tone, whereas when the intrinsic sinus node function is abnormal, the day to day variations during control state appear due predominantly to intrinsic sinus node abnormalities.     

Effects of pharmacologic autonomic blockade on atrial electrophysiologic properties in normal subjects and in patients with sinus node disease

In order to elucidate the influence of autonomic nervous system on atrial electrophysiologic properties, we studied 10 patients with sinus node dysfunction and 10 age-matched normal subjects. In each of them effective and functional refractory periods of the right atrium (near its junction with the superior caval vein) were measured, during atrial pacing (100/min) and using variable current strengths (2, 3, 4, 5, 7, 10, and 15 mA), before and after pharmacologic autonomic blockade (using intravenous propranolol 0.2 mg/kg and atropine 0.04 mg/kg). Mean values of effective and functional refractory periods at each current strength were significantly higher in patients with sinus node disease than in normal subjects both before and after autonomic blockade. Blockade did not significantly modify mean values of effective and functional refractory periods at any current strength, either in patients with sinus node disease or in normal subjects. Furthermore, autonomic blockade did not change the effects of the increase of current strength on atrial refractoriness in either group. We conclude that our data indicate a prolonged refractoriness to be present in patients with sinus node disease even in the absence of influences from the autonomic nervous system. Thus, we can suggest a "primary" involvement of atrial fibers in this pathophysiological condition. Propranolol together with atropine did not induce changes of atrial refractoriness. Indeed, they probably exerted an opposite effect. The effects of the increase of current strength on atrial excitability do not seem to be mediated by autonomic humoral agents.     

Diagnostic value pharmacological autonomic blockade in patients with suspected sick sinus syndrome

The study comprised 67 subjects, mean age 43.7 years, with suspected sick sinus syndrome, in whom rapid atrial pacing before and after combined atropine and propranolol was performed by Narula's method. Three groups were formed: group I--with normal sinus node recovery time (SNRT) and corrected sinus node recovery time (CNRT) before and after the autonomic blockade; group II--with functional disorders of the sinus node and group III--with intrinsic sinus node dysfunction. After autonomic blockade in groups I and II mean SNRT, CNRT, post-stimulation cycle lengths (except No. 2 and Nos. 5, 6, 10, respectively) shortened, whereas HR rose. In contrast, in group III mean SNRT, CNRT, post-stimulation cycle lengths (Nos. 1, 2, 6, 10) and HR increased. Significant differences in post-stimulation cycle lengths were observed between groups I and III as well as groups II and III. In conclusion, rapid atrial pacing after combined atropine and propranolol helps us to diagnose latent sick sinus syndrome and extrinsic sinus node dysfunction more precisely, and significant differences in post-stimulation cycle lengths between the groups confirm diagnostic value.     

Effect of pacing cycle length and autonomic blockade on sinus node refractoriness

Sinus node (SN) refractoriness can be measured indirectly by observing the return responses after the introduction of progressively earlier atrial premature beats. The SN effective refractory period (ERP) is defined as the longest premature interval resulting in an interpolated atrial return response. In the present study, SNERP was analyzed in 71 subjects--51 control persons and 20 patients with evidence of SN dysfunction. SNERP could be measured in 40 of 51 control subjects and was shown to prolong at shorter basic pacing cycle lengths. At a basic cycle length of 600 ms, SNERP was 330 +/- 40 ms, whereas at 500 ms it was 350 +/- 50 ms (p less than 0.05). At a basic cycle length of 600 ms, SNERP was measured in 31 control subjects and 7 patients with SN dysfunction. The values of 330 +/- 40 and 520 +/- 20 ms, respectively, in these 2 groups suggested that this method can be used to differentiate patients with SN dysfunction (p less than 0.001). In 12 control subjects, SNERP was measured before and after partial autonomic blockade with propranolol and atropine. SNERP shortened from 360 +/- 40 to 320 +/- 40 ms (p less than 0.05). It shortened with atropine and prolonged with propranolol. Thus, SNERP prolongs with a shorter basic pacing cycle length and is affected by autonomic manipulation, in a fashion analogous to the atrioventricular node.     

Is sick sinus syndrome an adenosine-mediated disease? Effects of intravenous aminophylline on sick sinus node function after pharmacologic autonomic blockade

To assess the effects of intravenous aminophylline on the sinus node, 12 patients with clinical and Holter monitor-documented sick sinus syndrome were studied (1) during the control state, (2) after pharmacologic autonomic blockade and (3) 5 min after intravenous administration of aminophylline. The effects of aminophylline on sinus node function were compared with those after pharmacologic autonomic blockade. No significant improvement of sinus node function was found after intravenous aminophylline administration with a mean sinus cycle length and a mean maximum CSRT of 968 +/- 218 and 1832 +/- 1036 ms, respectively. The mean serum theophylline level was 10.9 +/- 1.7 micrograms/ml. Since aminophylline is an adenosine receptor antagonist, these findings suggest that intrinsic adenosine may not play an important role in pathogenesis in patients with chronic and advanced sick sinus syndrome.     

Differential effects of autonomic blockade on sinus and atrioventricular nodal function in normals and in intrinsic sinus node dysfunction

The effect of pharmacologic total autonomic blockade on sinus and atrioventricular nodes was studied in 10 normals and 21 patients with sick sinus syndrome with abnormal intrinsic corrected sinus node recovery time. In normals the intrinsic heart rate (113.3 +/- 11.6 beats/min) was higher than the resting heart rate (87.3 +/- 12 beats/min; P less than 0.001). The AH interval at an identical paced rate decreased from 119 +/- 36 msec to 93 +/- 17.6 msec after autonomic blockade (P less than 0.05). Mean atrial paced cycle length at AH Wenckebach block was not different during control and after drugs (319 +/- 46 msec vs. 311.5 +/- 39 msec; P = NS). Although sinus cycle length shortened in all cases after autonomic blockade, paced cycle length at AH Wenckebach increased (4) or remained unchanged (3) in 7 cases. Maximum normal "intrinsic" paced cycle length at AH Wenckebach was 390 msec (mean +/- 2 SD). In sick sinus syndrome, resting heart rate (66.3 +/- 18.8 beats/min) and intrinsic heart rate (74.6 +/- 16.4 beats/min) were similar (P = NS); AH at identical paced rate: control 136.6 +/- 54 msec, after drugs 130.5 +/- 35 msec (P = NS); cycle length at AH Wenckebach: control 380.5 +/- 73 msec, after autonomic blockade 383 +/- 49 msec (P = NS). Two of 3 cases with abnormal atrioventricular nodal response to atrial pacing during control normalized after autonomic blockade; 9/21 (42.8%) cases developed AH Wenckebach at cycle length greater than 390 msec after autonomic blockade. The data suggest that the autonomic nervous system has differential effects on sinus and atrioventricular nodes. Patients with sick sinus syndrome frequently have abnormalities of "intrinsic" atrioventricular nodal conduction unmasked by autonomic blockade.     

Cardiac effects of acute ethanol ingestion unmasked by autonomic blockade.

We assessed the effects of ethanol and autonomic blockade on left ventricular function in nine normal subjects, age 20--35 years, using M-mode echocardiography and systolic time intervals. On day 1, measurements were made of heart rate, mean velocity of circumferential fiber shortening, and left ventricular pre-ejection period and left ventricular ejection time ratio (PEP/LVET), during a control period and after autonomic blockade. Autonomic blockade was produced with intravenous propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg body weight). On day two, measurements were again made during a control period, then with ethanol alone, followed by addition of autonomic blockade to ethanol. One hundred eighty milliliters of ethanol were ingested over 60 minutes, resulting in a mean blood ethanol level of 110 mg/dl (range 77--135 mg/dl) at 60 minutes post-ingestion. There were no significant differences between the control data on days 1 and 2. Blood pressure was unchanged throughout the study. study. On day 1, autonomic blockade alone resulted in the expected increase in heart rate (p less than 0.001), with a proportional increase in mean velocity of circumferential fibr shortening (p less than 0.01), and an increase in PEP/LVET (p less than 0.01). On day 2, ethanol alone resulted in no significant changes except for a slight increase in PEP/LVET (p less than 0.02). Ethanol plus autonomic blockade, (day 2), compared with autonomic blockade alone (day 1), revealed a decrease in mean velocity of circumferential fiber shortening (p less than 0.05), and an increase in PEP/LVET (p less than 0.01), with a decrease in intrinsic heart rate (p less than 0.001). We conclude that in normal subjects: 1) autonomic blockade does not directly affect contractility; 2) acute ethanol ingestion alone does not produce important changes in cardiac function; and, 3) ethanol in the autonomic blockaded heart causes a significant decrease in contractility. Thus, we infer that ethanol has a negative inotropic effect which is masked by catecholamines and/or autonomic nervous system discharge.     

Differential effects of functional autonomic blockade on the variables of sinus nodal automaticity in sick sinus syndrome

To study the pathophysiologic mechanism of sick sinus syndrome and to establish the relation of intrinsic heart rate, corrected sinus nodal recovery time and sinoatrial conduction time in this syndrome, electrophysiologic studies were conducted in 22 men (mean age 60 ± 12 years) with the clinical diagnosis of sick sinus syndrome. Measurements were determined before and after autonomic blockade with propranolol (0.2 mg/kg body weight) and atropine sulfate (0.04 mg/kg). Fifty-nine percent of patients (Group I) had an abnormal intrinsic heart rate, suggesting intrinsic abnormality of sinus nodal automaticity; 41 percent (Group II) had a normal intrinsic heart rate after autonomic blockade, suggesting disturbed autonomic regulation. One patient with an observed intrinsic heart rate higher than the upper limit of predicted intrinsic heart rate was also included in Group II. The mean corrected sinus nodal recovery time before autonomic blockade was 751 ± 502.8 ms and was abnormal (more than 450 ms) in 10 of the 13 patients in Group I and 2 of the 9 patients in Group II. After autonomic blockade this interval was 694 ± 638.7 ms and was abnormal in 12 of the 13 patients in Group I and in 2 of the 9 patients in Group II. The patients in each group could be further classified into three groups on the basis of normal or abnormal corrected sinus nodal recovery time before or after autonomic blockade. Not all patients with abnormal intrinsic heart rate (Group I) had abnormal corrected sinus nodal recovery time and vice versa. Patients in Group II were younger in age, had a lesser incidence of organic heart disease and were more severely symptomatic.Mean sinoatrial conduction time during control studies was 210.4 ±96.3 ms and decreased significantly (143.2 ± 59.6 ms, p < 0.005) after autonomic blockade. This interval was abnormal in 3 of the 13 patients in Group I and in 6 of the 9 patients in Group II during control studies; after autonomic blockade it remained abnormal in 3 patients in Group I and in 1 patient in Group II.It is concluded that determination of heart rate and corrected sinus nodal recovery time after autonomic blockade increases the sensitivity of electrophysiologic testing and offers some insight into the pathophysiology of sick sinus syndrome. Patients with sick sinus syndrome who have a normal intrinsic heart rate have a greater incidence of abnormal sinoatrial conduction time than do those with an abnormal intrinsic heart rate. Thus, abnormal sinoatrial conduction time is usually due to extrinsic autonomic influences.     

Lithium-induced sinus node disease at therapeutic concentrations: linking lithium-induced blockade of sodium channels to impaired pacemaker activity

The present report describes a case of sinus node arrest in a manic-depressive patient being treated with lithium carbonate with a therapeutic serum level of lithium. A permanent rate-modulated ventricular pacemaker was inserted and lithium therapy was continued. A review of literature revealed several other similar case reports in which both therapeutic and toxic levels of serum lithium levels were associated with sinus node dysfunction and bradyarrhythmias. Because lithium is a potent blocker of cardiac sodium channels, and given the critical importance of sodium channels in pacemaker activity, lithium-induced sodium channel blockade is likely an important mechanism in sinus node dysfunction.     

Hemodynamic influences on sinus node recovery time: effects of autonomic blockade

Ten patients with normal sinus node function were evaluated prospectively, to determine whether the decrease in blood pressure during rapid atrial pacing shortens the corrected sinus node recovery time. All patients had 30 seconds of atrial pacing at cycle lengths from 600 to 300 ms, with continuous arterial pressure monitoring, before and after intravenous administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In the control state, a decrease in corrected sinus node recovery time was recorded with faster atrial pacing rates, which was significantly related to the initial drop in systolic blood pressure at the onset of atrial pacing. Specifically, as the initial pressure drop increased from 15 mm Hg or less to 16 to 45 and 45 to 100 mm Hg, corrected sinus node recovery time decreased from 272 +/- 79 to 205 +/- 70 ms (p less than 0.04) and to 134 +/- 120 ms (p less than 0.04), respectively. In contrast, after autonomic blockade, the corrected sinus node recovery time was prolonged, in a near linear fashion, as atrial pacing rates increased. The magnitude of blood pressure drop with atrial pacing did not differ significantly from that in the control state at similar pacing rates. These findings suggest that hypotension during rapid atrial pacing activates autonomic reflexes that significantly shorten the corrected sinus node recovery time. Autonomic blockade negates this effect and the corrected sinus node recovery time prolongs with faster atrial pacing.     

Cardiac autonomic modulation in hypertensive patients with Chagas' disease

BACKGROUND: Arterial hypertension and Chagas' disease are prevalent pathologies in Latin America. It has been demonstrated that each one of them may cause cardiac autonomic dysfunction. This study aimed to investigate the pattern of cardiac autonomic modulation in chagasic-hypertensive patients. METHODS: Subjects (n=120) without left ventricular dysfunction were distributed in four groups: healthy control (n=30); hypertensive (n=30); chagasic (n=30) and chagasic-hypertensive (n=30). Patients were evaluated by autoregressive spectral analysis of heart rate variability in three different conditions: baseline, cold face and passive tilt tests. Power spectral densities in low (0.04-0.15 Hz) and high (0.15-0.50 Hz) frequency bands were estimated in both absolute and normalized units. RESULTS: Baseline median values (percentile 25 to percentile 75) of mean arterial pressure (in mmHg) were 93.3 (85.0-96.7), 116.7 (*, #) (110.0-129.2), 86.7 (83.3-92.5) and 106.7 (*, #) (106.7-110.0) for healthy control, hypertensive, chagasic and chagasic-hypertensive patients, respectively (*p<0.05 versus healthy control, #p<0.05 against chagasic group). Heart rate at rest did not differ among groups. Regarding to spectral parameters in baseline conditions, the absolute power of high frequency component of heart rate variability of the chagasic-hypertensive group was significantly lower than that found in healthy control and hypertensive patients. There were no differences in spectral parameters responses during cold face test. After passive tilt test, however, decreases in high frequency oscillations and increases in sympathovagal balance (low and high frequency ratio) were significantly lower in hypertensive, chagasic and chagasic-hypertensive patients as compared with healthy control. CONCLUSIONS: These data indicate that chagasic-hypertensive patients presented an impairment of cardiac parasympathetic modulation at baseline conditions as well as in response to passive orthostatic stress.     

Cardiac autonomic dysfunction in patients with gastroesophageal reflux disease

AIM: To investigate autonomic nervous function in patients with a diagnosis of gastroesophageal reflux disease(GERD).METHODS: The investigation was performed on 29patients(14 men), aged 18-80 years(51.14 ± 18.34),who were referred to our Neurocardiology Laboratory at the Clinical and Hospital Center "Bezanijska Kosa"with a diagnosis of GERD. One hundred sixteen healthy volunteers matched in age and sex with the examinees served as the control group. The study protocol included the evaluation of autonomic function and hemodynamic status, short-term heart rate variability(HRV) analysis, 24 h ambulatory ECG monitoring with long-term HRV analysis and 24 h ambulatory blood pressure monitoring.RESULTS: Pathologic results of cardiovascular reflex test were more common among patients with reflux compared to the control group. Severe autonomic dysfunction was detected in 44.4% of patients and in7.9% of controls(P 0.001). Parameters of short-term analysis of RR variability, which are the indicators ofvagal activity, had lower values in patients with GERD than in the control group. Long-term HRV analysis of time-domain parameters indicated lower values in patients with reflux disease when compared to the control group. Power spectral analysis of long-term HRV revealed lower low- and high-frequency values.Detailed 24 h ambulatory blood pressure analysis showed significantly higher values of systolic blood pressure and pulse pressure in the reflux group than in the control group.CONCLUSION: Patients with GERD have distortion of sympathetic and parasympathetic components of the autonomic nervous system, but impaired parasympathetic function appears more congruent to GERD.     

Effects of digitalis on the human sick sinus node after pharmacologic autonomic blockade

To study the effects of digitalis on the sinus node and the mechanisms involved, 16 patients with the sick sinus syndrome had electrophysiologic assessment of sinus nodal function during (1) control study, (2) after pharmacologic autonomic blockade with propranolol (0.2 mg/kg body weight and atropine sulfate 0.04 mg/kg intravenously), and (3) 10 minutes after 0.01 mg/kg of intravenous ouabain. The study was completed within 30 minutes of pharmacologic autonomic blockade. During the control study 50 percent of patients had an abnormal corrected sinus nodal recovery time or abnormal sinoatrial conduction time, or both. The effects of ouabain on sinus nodal function were compared with those after pharmacologic autonomic blockade. Ouabain significantly increased both intrinsic sinus cycle length (ouabain 975 ± 194 ms [mean ± standard deviation]; autonomic blockade 1,025 ± 218 ms, probability [p] < 0.001) and corrected sinus nodal recovery time (ouabain 615 ± 503 ms; autonomic blockade 575 ± 536 ms, p < 0.05). In contrast there was no significant change in sinoatrial conduction time after ouabain (ouabain 141 ± 56 ms; autonomic blockade 132 ± 45 ms; difference not significant). The effects of ouabain were similar in patients with both normal and abnormal sinus nodal function.These findings suggest that (1) digitalis in therapeutic doses has a depressant effect on intrinsic sinus nodal automaticity in patients with normal as well as abnormal sinus nodal function; (2) digitalis has no significant effects on sinoatrial conduction; and (3) the effects of digitalis on sinus nodal automaticity are primary and independent of its vagal and antiadrenergic effects.     

Electrophysiologic evaluation of sinus node dysfunction in postoperative children and young adults utilizing combined autonomic blockade

Sinus node dysfunction is a recognized problem following surgery for congenital heart disease. Seven postoperative patients with sinus node dysfunction (5 Mustard, 1 tetralogy of Fallot, 1 Fontan) underwent electrophysiology study of sinus node function during combined autonomic blockade (CAB) utilizing propranolol 0.2 mg/kg i.v. and atropine 0.04 mg/kg i.v. to evaluate intrinsic sinus node function isolated from autonomic control. During CAB, intrinsic heart rate, intrinsic corrected sinus node recovery time, and intrinsic sinoatrial recovery time were measured. These results were compared with age-matched normal intrinsic data from our lab [normal (n = 7, mean age 9 years) IHR 128 +/- 24, intrinsic corrected sinus node recovery time 135 +/- 40 ms, intrinsic sinoatrial conduction time 86 +/- 19 ms]. Among postoperative Mustard patients (n = 5, mean age 13 years, mean years postoperative 11) 2 of 5 had clearly abnormal intrinsic sinus node function with nonsinus rhythm during CAB; 3 of 5 had sinus rhythm during CAB with normal or mildly abnormal intrinsic sinus node function. The postoperative case of tetralogy of Fallot (age 20 years, postoperative 14 years) had mildly abnormal intrinsic sinus node electrophysiology study. The postoperative case of Fontan (age 16 years, postoperative 1.5 years) had sinus rhythm at rest but left atrial rhythm during CAB. Different aspects of sinus node dysfunction may be expressed during resting electrophysiology study vs. electrophysiology study utilizing CAB. The pathophysiology of sinus node dysfunction among postoperative pediatric patients is not homogeneous with regard to the contribution of intrinsic sinus node dysfunction. In those patients with normal or mildly abnormal intrinsic sinus node function, an important pathophysiologic influence of the autonomic nervous system is implicated.     

Cardiac autonomic dysfunction and neuroganglionitis in a rat model of chronic Chagas' disease.

OBJECTIVE: The aim was to evaluate whether the cardiac parasympathetic function in a rat model of chronic Chagas' disease is impaired as in the human disease, and to correlate the functional state to histopathology of the intrinsic autonomic innervation of heart. METHODS: 70 male Wistar rats 8 months infected with strains Y (n = 22), S?o Felipe (n = 18), and Colombia (n = 30) of Trypanosoma cruzi, were compared with 20 age and sex matched non-infected controls. Baroreflex bradycardia was quantified after multiple bolus injections of phenylephrine (3 to 12 micrograms). For each rat studied a mean was obtained of the absolute and relative (delta %) ratio (index) between the maximum heart rate decrease and the maximum systolic blood pressure increase. RESULTS: For the relative index the means were smaller (p less than 0.05) in the Y [-0.52(SD 0.19)%], S?o Felipe [-0.45(0.28)%], and Colombia [-0.53(0.21%)] subgroups, as well as in the pooled chagasic group [-0.51(0.22)%], than in the control group [-0.64(0.13)%]. In 32% (7/22), 33% (6/18), and 20% (6/30) of rats infected with Y, S?o Felipe, and Colombia strains, respectively, and in 27% (19/70) of the pooled group rats, the index exceeded the control group mean by -2 SD. After atropinisation, a similar pronounced reduction (p less than 0.01) in the index was observed in all groups [-84(28)% to -95(17)%]; however, rats with depressed bradycardia showed a smaller (p less than 0.05) reduction in the relative index than control rats, at -70(34) v -92(16%). Inflammatory and degenerative lesions of the intrinsic cardiac innervation were observed in 87% of the rats with autonomic dysfunction. Rats with the lesions showed a mean relative index that was smaller than those without lesions, at -0.44(0.23) v -0.64(0.20)% (p less than 0.01), and also smaller than in the controls. CONCLUSIONS: Cardiac autonomic dysfunction expressed by reduced baroreflex bradycardia was detected in rats chronically infected with T cruzi, as in human Chagas' disease. The disturbance, shown for the first time in an animal model of chagasic infection, resulted primarily from impaired efferent parasympathetic activity caused by intrinsic neuroganglionar lesions.     

Pacemaker pseudodysfunction with a coronary sinus pacemaker

A permanent transvenous coronary sinus pacemaker functioned effectively for 22 months both as an atrial and ventricular pacemaker. Slow atrial flutter resulted in failure of the pacemaker to capture the myocardium and thus incorrectly suggested pacemaker dysfunction. Transtelephonic evaluation of this phenomenon was particularly difficult and could have resulted in unnecessary replacement of the pacing unit     

Effect of the autonomic blockade on the automaticity of the A-V junctional pacemaker in awake dogs.

The effect of the autonomic blockade on the automaticity of the A-V junctional pacemaker was evaluated in 15 awake dogs with experimentally induced A-V junctional rhythm. The duration of asystole after overdrive (D.A.O.) in these dogs was prolonged significantly in accordance with increase in the drive rate, and the mean +/- SD of the D.A.O. reached 4.7 +/- 1.1 seconds (N = 15) after overdrive at 2.5 times the spontaneous heart rate. After administration of atropine (0.4 mg/kg; i.v.) to eight dogs, the mean +/- SD of the D.A.O. at the same rate decreased from 4.5 +/- 0.9 to 3.4 +/- 1.2 seconds. After administration of practolol (0.5 mg/kg; i.v.) to the seven other dogs, the mean +/- SD of the D.A.O. at the same rate increased remarkably from 4.9 +/- 1.3 to 9.4 +/- 3.0 seconds. Intravenous injection of practolol (0.5 mg/kg) had no effect upon the D.A.O. in the five dogs with sinus rhythm. Thus, it is suggested that (1) the sympathetic nerve might play a more important role in regulating the automaticity of the A-V junctional pacemaker than the vagus and (2) it physiologically might take over 5.0 seconds for the A-V junctional pacemaker to initiate an escape beat during longstanding sinus arrest, if a marked dysfunction of the A-V junctional pacemaker occurs due to a decrease in tension of the sympathetic nerve.